lupron side effects Archives - Page 2 of 3

Lupron, Surrogacy, and Multiple Sclerosis White Matter Lesions

Published on November 21, 2022

8465 views

I decided to be a surrogate after watching a birth story on TV. I felt like it would be a meaningful way to give back. I was adopted as an infant and I wanted to help another couple have a baby of their own. I did some research, found an agency, met a couple, and went through reproductive screening at a fertility clinic. They explained to me that they would give me hormone injections to artificially stop my body from releasing an egg. I was a gestational surrogate, meaning I only carried the embryo. The embryo was made from a donor egg. Once they confirmed that I had not ovulated they would begin giving me estrogen to produce a uterine lining. After two weeks, it was time for the big day, the transfer of the embryo to my uterus. The embryo transfer was successful and so for twelve weeks following I took a daily injection of progesterone.

I am ashamed to say that I did not do my research and I did not know exactly what I was taking, other than “hormones”. I recall the potential side effects being listed as headache, fatigue and hot flashes and that these side effects were temporary and would dissipate after I stopped taking the medication. I remember glancing over the package insert for the leuprolide acetate (Lupron) noticing nothing was too alarming.

Post Lupron Symptoms

I went on to deliver a healthy baby boy in May of 2013, his parents were thrilled and it was time to focus on me again, get my body back in shape and move on with my life. It was August when I had my first “attack”. I was feeling extremely dizzy and had tingling in my left hand so I went to my primary care provider. She could not tell exactly what was going on but felt that the dizziness was caused by allergies and the numbness in my left arm caused by carpel tunnel. She sent me home with an antihistamine and a brace for my left arm. Eventually my symptoms subsided and I felt perfectly normal.

In January of 2014, I began feeling dizzy again, I tried an antihistamine and it just made me tired. The tingling and numbness came back in my left hand. I went to a different doctor who told me I had vertigo. The doctor tried a few tricks, such as hanging upside down and flipping up really quickly to try to “reset” my equilibrium (that didn’t work). The tingling in my arm was thought to be a pinched nerve in my neck because I lifted weights. Several days went by and I was still feeling terrible, the numbness was also occurring in my face. I was convinced I was having a stroke or that I had brain tumor. I went back to the doctor, insisting on an MRI. I was relieved when I was told that I did not have a tumor. The doctor said that I had signs of a demyelinating disease, such as multiple sclerosis. There are six lesions on my brain.

Multiple Sclerosis or Something Else?

Obtaining the actual diagnosis was a very long process which involved a lumbar puncture to check my cerebrospinal fluid for elevated levels of antibodies and a specific group of proteins called oligoclonal bands. The findings indicated I did have elevated levels of the antibodies but that the group of proteins were not present. Still the neurologist felt that it was enough for a diagnosis for multiple sclerosis and prescribed a disease modifying drug, a three times a week injection. Multiple sclerosis cannot be cured but there are drugs designed to try to prevent the immune system from attacking the myelin sheath (protective nerve coating). I sought the opinion of another neurologist who had a specialty in multiple sclerosis. She agreed with the diagnosis of Relapsing Remitting Multiple Sclerosis, which is characterized by clearly defined attacks of new or increasing neurologic symptoms. These attacks are followed by periods of partial or complete recovery. During remissions, all symptoms may disappear, or some symptoms may continue and become permanent. However, there is no apparent progression of the disease during the periods of remission.

Another Surrogacy and Another Round of Lupron

During this process, I knew that I was going to be gestational surrogate again. I had already committed to the couple to carry a second child for them. I stopped taking my disease modifying drug and began the gestational surrogacy protocol again of Lupron, estrogen and progesterone. Thankfully we were successful on the first round as we were with the first baby. Many surrogates are not successful on the first round and go through the protocol over and over again.

I was advised by my neurologist that many women have an exacerbation of MS after birth, as it is very stressful on the body. He advised that I begin taking steroids immediately following the birth to prevent a relapse. I had a very traumatic birth, resulting in surgery and I decided I did not want to take steroids. I would take my chances with the relapse – nothing happened, I felt perfectly normal again.

I am currently not treating myself with the medication prescribed for MS. I have not had any new or worsening symptoms in three years and each MRI shows no new lesions, although I live daily with existing symptoms. I have damage to my trigeminal nerve causing constant pain and numbness in the left side of my face, I also have occasional numbness and tingling in my left arm and leg.

When I was first diagnosed, I searched for nearly every cause I could think of. There is no one in my family history with MS. I didn’t have a vitamin D deficiency. I didn’t have the Epstein-Barr virus or any of the other things thought to be linked to multiple sclerosis. I started searching though my life for anything unusual, which is when I finally researched Lupron. There have been less than 5% of adverse effects reported; however, neuromuscular conditions are listed. I have since learned that there are no clinical studies on the safety of Lupron for IVF and it is being used as an “off label” medication. This allows for it to be used for medical purposes that were not originally specified in the FDA’s approval of the drug and it is not on the labeling. I have reached out to many women online and have heard similar stories of MS, or MS like symptoms or other autoimmune conditions and the use of Lupron.

I feel that I was lucky, I only took Lupron for a short amount of time, many women take it for much longer and at higher doses, possibly causing more damage. I want women, potential surrogates, reproductive endocrinologists and fertility clinics to be aware of this. I want more research to be done on the hazards of the drug. I want to prevent the off-label use of medications.

Share Your Story

If you have experience with Lupron and/or with surrogacy would like to share your story, send us a note.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

This article was published originally on February 13, 2018.

Tank Estradiol and Lose Metabolic Flexibility: Pitfalls of Lupron and Oophorectomy

by Chandler Marrs, PhD

Published on August 2, 2022

13933 views

Over the last several weeks, I have been looking at the role of estradiol in mitochondrial health. In the first post Hormones, Hysterectomy and the Aging Brain, we learned that estradiol depletion wreaks havoc on brain mitochondria turning them into misshapen donuts and blobs. Digging a little deeper, the next post (Lupron, Estradiol and the Mitochondria) pondered the connection between estradiol-depleting drugs such as Lupron, other Lupron-like drugs, and the devastating side effects that often follow suit. Could Lupron-mediated mitochondrial damage be at the root of these side effects? Quite possibly? A question that remains is how. In this post, I will be digging even deeper into the role of estradiol in mitochondrial functioning, especially its role in something called metabolic flexibility.

A note of caution, while I focus on estradiol, the mitochondria, and what happens to health when we remove estradiol pharmaceutically via Lupron or surgically via oophorectomy, it is important to remember that estradiol is not the only hormone synthesized in the ovaries nor are the ovaries the only hormone-producing tissues. Moreover, the chemical castration induced by Lupron and other medications or via ovary removal disrupts and diminishes the synthesis of a myriad of hormones. Estradiol is simply where most of the research is focused, and so, it is where I too must focus, at least for the time being.

Steroid Hormones and Metabolic Flexibility: A Critical Factor in Post Lupron and Post Oophorectomy Ill Health

Steroid hormones regulate metabolic flexibility at the level of the mitochondria. Estradiol, the most frequently studied among the steroid hormones, plays a pivotal role in determining how food fuel is converted into cellular fuel or ATP. When we eliminate estradiol with medications such as Lupron and other GnRH agonists or antagonists, or when we remove a woman’s ovaries, depleting her primary source for estrogen synthesis, metabolic flexibility diminishes significantly. With the lack of metabolic flexibility comes several health issues, some noticeable, like weight gain, and others less noticeable, at least initially, like cardiac and neurodegenerative diseases. A common component of each of these conditions is mitochondrial dysfunction. Mitochondrial dysfunction can be initiated and accumulated via a number of mechanisms and over time, so estradiol is not the only variable, but it is a key factor that is often ignored.

Mitochondria

Mitochondria are the cellular powerhouses that consume oxygen and transform the foods we eat into a currency that cells can use (ATP) to perform all of the intricate tasks needed for survival and health. Mitochondria are also the site of steroidogenesis (steroid synthesis), immune signaling, and all sorts of other functions that determine cellular life and death. When you think about it, how well the mitochondria perform these tasks affects health at every level of organismal physiology. Without the appropriate amount of mitochondrial energy/ ATP, cell function becomes deranged, and ultimately, grinds to a halt. When that happens, disease is imminent. Indeed, genetic perturbations of mitochondrial function are some of the most devastating diseases known to medicine.

One has to wonder, what happens when we perturb mitochondrial function from the outside in – via toxicant exposure or by eliminating critical hormones or other co-factors such as nutrients that are necessary to mitochondrial operations? Worse yet, what if an individual with unrecognized genetic defects in mitochondrial functioning faces additional mitotoxicant exposures; what then? Complex, multi-system disease – that’s what. I would argue that mitochondrial dysfunction represents the final common pathway, a convergence point, connecting an array of seemingly disparate disease processes. Mitochondrial metabolism, and specifically, metabolic flexibility, may be at the heart of the derangement, with estradiol, and likely other hormones, in the driver’s seat.

Metabolic Flexibility: Adapt and Survive

When we think of stress and flexibility in general terms, it is easy to recognize that the more flexible one is in his/her behaviors or coping mechanisms, the easier it is for one to respond to, and survive stressors. Flexibility means that options exist for when everything hits the fan. Imagine if there were no options or if you had to respond to each and every stressful event in your life using exactly the same behaviors or response patterns. You would not get very far. The same holds true for cell behavior, and more specifically, mitochondrial behavior. The mitochondria need options to respond to the differing needs of the cells that they supply with energy. If those options become limited in any way, the mitochondria become less effective. They produce less energy, scavenge fewer oxidants (toxicants), and when stressors present, cannot easily adapt. In fact, the more inflexible the mitochondria are forced to become, the less likely they, and the cells, tissues, organs, and organism within which they reside, will survive. Estradiol is integral to mitochondrial flexibility. Remove the estradiol and the mitochondria become less metabolically flexible and less able to respond to the demands of a changing environment.

Estradiol Equals Increased Mitochondrial Efficiency and Decreased ROS

Estradiol maintains metabolic flexibility via two important mechanisms: increased mitochondrial efficiency and ROS management. With the former, estradiol regulates metabolic flexibility by altering the expression of genes that control the enzymes within the fuel conversion pathways. It is a complex algorithm of responses, with some proteins upregulated and others downregulated. The net result, however, favors increased efficiency in ATP production by maximizing metabolic flexibility or adaptability to the environment.

With the latter, estradiol, along with progesterone, manage the clean-up tasks inherent to any energy production process. In effect, estradiol manages ROS both on the front end and the back end of mitochondrial ATP production. On the front end, increased metabolic efficiency and flexibility equals fewer ROS byproducts. On the backend, estradiol cleans up the byproducts of processing -ROS – and tempers the damage these byproducts can cause.

Estradiol, Pyruvate, and ATP

Of particular interest to our work here at Hormones Matter, estradiol upregulates a set of enzymes called the pyruvate dehydrogenase complex, PDC. The PDC, responsible for converting glucose into pyruvate, is the first step in the long process that nets multiple units of mitochondrial ATP. The PDC is key to carbohydrate metabolism and more recently has been linked to fatty acid metabolism, making this enzyme complex central to mitochondrial energy production. Diminished PDC derails mitochondrial functioning, producing serious diseases. Children born with genetic pyruvate dehydrogenase deficiency suffer serious neurological consequences and rarely live to adulthood.

Importantly, the PDC (like all of the enzymes within these cascades) is highly dependent upon nutrient co-factors to function properly. Thiamine and magnesium, are critical to the PDC complex. Since PDC function demands thiamine, children and adults with thiamine deficiency also suffer significant ill-health, ranging from fatigue and muscle pain, to disturbed cognitive function, disrupted autonomic function affecting multiple organs, psychosis, and even death if not identified. Thiamine deficiency is most well known as a disease associated with chronic alcoholism but has recently begun re-emerging in non-alcoholic populations relative to medication and vaccine reactions. Many medications and environmental variables deplete thiamine and magnesium, diminishing mitochondrial function significantly, by way of pyruvate.

Along with nutrient co-factors, estradiol is critical for pyruvate. Estradiol upregulates the expression of the enzymes that make up the PDC (in the brain). If estradiol is reduced or blocked, mitochondrial ATP production will take a hit. If estradiol is blocked in an already nutrient-depleted woman, the first step in mitochondrial fuel conversion would take a double hit. One can imagine the consequences.

In light of the direct role that thiamine, magnesium, and other nutrients play in the cascade of reactions required to produce ATP, can we maximize mitochondrial functioning with nutrients to compensate for the mitochondrial damage or deficiencies likely to occur post oophorectomy or as a result of GnRH agonist or antagonist drugs, like Lupron? I can find no research on the subject, but it is certainly a topic to explore given the millions of women already suffering from the mitochondrial damage induced by Lupron and/or pre-menopausal ovary removal. Even without the necessary research, correcting nutrient deficiencies and dietary issues should be undertaken for general health.

Another question in need of exploration, if we maximize mitochondrial functioning, does that then increase steroidogenesis in other endocrine glands? A section of the adrenal glands called the zona reticularus, for example, produces a complement of hormones similar to those of the ovaries. In postmenopausal women androgens, precursors for estradiol, produced by the adrenals account for a large percentage of total estradiol production. Could we take advantage of that to help stabilize circulating hormones?

Finally, beyond the nutrient requirements for mitochondrial ATP production, enzymes throughout the body, even those involved in post-mitochondrial steroid metabolism, require nutrient co-factors to function properly. Could we maximize those enzymes for more efficient steroid metabolism to net sufficient estradiol to maintain mitochondrial function?

What about Natural Declines in Estradiol?

It is not clear how menstrual cycle changes in estradiol affect mitochondrial functioning or how the postpartum decline in pregnancy hormones affects mitochondria. One would suspect there are compensatory reactions to prevent damage, but this has not been investigated. In natural menopause, however, researchers have noted that some form of compensation occurs as estradiol declines and, at least for a time, and in rodents, mitochondria maintain efficient production of ATP. In contrast, no such changes are noted with premature menopause or oophorectomy.

Also not investigated sufficiently, is the impact of chronic synthetic estrogen exposure on mitochondrial functioning. In other words, what are the effects of oral contraceptives, HRT, and the growing list of environmental endocrine disruptors, on mitochondrial ATP production? Since these compounds bind to estrogen receptors and displace the endogenous estrogens like estradiol, some evidence suggests endogenous production of estradiol is reduced. Do the mitochondria respond also by downregulating estrogen receptors or by some other mechanism? Short-term, animal research suggests that supplementing 17B estradiol post oophorectomy reduces mitochondrial damage. In research in humans, where synthetic estrogens are used, results are less clear and longer-term studies do not exist beyond the broad brush strokes of epidemiology.

Metabolic Flexibility and Tissue Type

One of the more interesting aspects of estradiol’s role in metabolic flexibility is that it is site or tissue-specific and may point to novel therapeutic opportunities. Since different cell types, in different parts of the body, prefer different fuels for power to survive, when we eliminate estradiol from the equation, mitochondria from different tissues or organs respond differently to the lack of flexibility. Perhaps, we can utilize the information about fuel requirements to design diets that compensate for diminished metabolic flexibility.

Heart Cells. I’ve written about this research previously, not fully understanding the implications. Estradiol allows cardiomyocytes (heart cells) to switch from their preferred fuel of fatty acids to glucose during stressors such as heart attacks (and theoretically during any stressor like exercise). That ability to switch fuel types is protective and allows the cells to survive and heal. It may explain why women are more susceptible to heart damage post-menopause when endogenous estradiol declines. This may also point to a pathway for post oophorectomy and post Lupron declines in normal heart function.

Brain Health. Declining estradiol affects brain mitochondria differently. As I noted in a previous post, without estradiol, brain mitochondria become progressively less functional and misshapen. These structural changes impair mitochondrial ATP production. Unlike the heart, however, the brain prefers glucose as its primary fuel source. Estradiol appears to enhance glucose uptake from the periphery and across the blood-brain barrier. When estradiol is absent, brain glucose uptake diminishes significantly (in rodent studies), leaving the brain perpetually starved for glucose.

We know from brain cancer research, that with declining brain glucose, secondary fuels can kick in, but only when the mitochondria have sufficient flexibility to switch. For example, mitochondrial fuel flexibility is critical to battling brain tumors. Under conditions of stress and when brain glucose concentrations are low, healthy mitochondria can readily transition to ketone bodies for energy, at least in vivo. The transition from glucose to ketone bodies is believed to be an evolutionary adaptation to food deprivation allowing the survival of healthy cells during severe shifts in the nutritional environment. Estradiol appears to be key in maintaining that flexibility.

Weight Gain and Fat Accumulation. Post-menopausal, post-hysterectomy, and oophorectomy weight gain are well established research findings. Anecdotal complaints of Lupron weight gain are also common. These findings may be related to derangements in metabolic flexibility mediated by the relationship between estradiol and mitochondrial functioning. The increased lipid or fat accumulation in skeletal muscle though associated with impaired insulin-stimulated glucose metabolism may be related to the reduced capacity to adjust to a changing fuel environment. More specifically, weight gain may represent a declining ability to utilize fats effectively as a mitochondrial fuel source, possibly via a derangement in a mitochondrial channel responsible for shuttling fats and cholesterol into the mitochondria for processing. When the mitochondria become less flexible, a channel called the TSPO, shuts down, disallowing fats that would normally be shuttled into the mitochondria and processed for ATP (and steroid hormones), from entering. Instead, they are stored peripherally in adipocytes. I wrote about this in detail here: It’s All about the Diet: Obesity and Mitochondrial Dysfunction. It is possible in estradiol-depleted women that TSPO downregulation is a compensatory reaction to diminished metabolic flexibility.

It is also conceivable that the lack of brain glucose, as discussed above, leads to overeating and, more specifically, cravings for sugary foods. This would be a logical compensatory reaction to bring more fuel to the brain; one likely meant only for the short term and that when held chronically begins the cascade of other metabolic reactions known as obesity, diabetes, and heart disease. Perhaps, just as fat storage becomes a survival mechanism when mitochondria can longer process it effectively, the craving for sugar in estradiol-deprived women is also a survival mechanism.

Finally, adipocytes can synthesize estradiol. It is conceivable that in response to declining estradiol concentrations, the body stores fat to produce more estradiol.

Final Thoughts

Central to mitochondrial dysfunction, whether by genetic predisposition or environmental influence, is the inability to efficiently produce ATP (the fuel that all cells need to survive) and to effectively manage the by-products of fuel production and other toxicants. Estradiol plays a huge role in both of these processes. Eliminate estradiol and mitochondrial functioning becomes less efficient and less flexible initiating cascades of chronic and life-altering conditions. This suggests the ready application of medications like Lupron that deplete estradiol or the prophylactic removal of women’s ovaries is misguided at best, and dangerous at worst.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, and like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Image by Triggermouse from Pixabay.

This post was published originally on Hormones Matter on February 11, 2015.

Short and Long Term Consequences of Lupron for Precocious Puberty

by Jody

Published on March 21, 2022

8775 views

As a child, at around age 5, I started experiencing severe pain in my legs and back. I had migraines from hell that made me feel as if my head were going to explode. I had hair in places that no five-year-old should and I needed a bra for kindergarten. I looked down on all my peers because I was a good 12 inches taller than most of them. I always had to be the mom when playing house in kindergarten. My parents struggled to find help for me because no doctor could explain why I hurt and felt the way I did. Finally, after being hospitalized for over a week my parents had answers. I was diagnosed with a hormone imbalance. The doctors in the area where I lived had no answers about how to treat me, so I was sent to a specialist in Augusta Georgia. He then called my diagnosis precocious puberty, a hormonal imbalance. After more needles and tests, he decided to start me on Lupron.

I took Lupron as a child from 1989 to 1994 for my hormone imbalance. I received a shot once a month in my thigh and sometimes in my butt cheek. I can remember the burn of the Lupron going into my body like it was yesterday. The injection always took me a week to recover from. I experienced soreness in the injection spot and redness every time I received Lupron. I could not run and play as a child. My legs either hurt or my mind would make me feel as though I had no purpose. From the outside, the Lupron shots were a success. The shots slowed my abnormal hair growth in private places and stopped my breast from growing, but on the inside, where it counts, what was the Lupron doing to me?

After being on the Lupron for half a year, I had lumps in my thighs where I received the injections (which I still have today). One time it crippled my legs, leaving me on crutches for two months when I was 7 years old. Yet still, I guess my doctor felt it would be more beneficial for me to continue my treatment with the Lupron because I received injections for 3 to 4 more years.

While on Lupron, I struggled daily to focus. I had blurred vision. I battled depression and I hurt daily. I couldn’t be active in sports due to my low bone mass and what kid feels like playing ball when her body feels like it’s been beaten with the bat already? By age 11, I finished up my treatment. I saw my doctor a handful of times after and then I was written off as cured, and I did feel good and enjoyed life for a few years.

At age 15, I began to battle depression. I struggled to remember things. I was diagnosed with asthma. My sight was getting worse and I had an eating disorder where I never wanted food due because my stomach felt like someone was squeezing it with all their might. I fainted several times because I was dizzy. I struggled to stand and I would walk holding onto things. My legs, arms, fingers, and toes would tingle and go numb. My doctor at the time seemed to always just prescribe me Lortabs for the pain and never dug any further to figure out why I felt the way I did. At age 17, I overdosed on Lortabs not trying to hurt myself but only trying to find relief from the pain. I didn’t realize that my body couldn’t handle all the medicine I was putting into it. My mom found me in my room and rushed me to the hospital where my stomach was pumped and I had to drink this disguising chalky drink. My pain seemed to decrease shortly after I turned 20. I looked and felt like the average healthy person. I had my first baby at 21 and my second at age 22. I had healthy pregnancies and healthy babies. I had my third baby at age 32 and again I was a healthy mama and had a healthy baby.

For the past two years, however, I have been experiencing a pain that is all too familiar. I feel as though my body and mind are failing me. I cannot pinpoint why all of this is happening to me. I am now 34 years old and experiencing horrific body aches and pains. I’m searching for answers as I struggle to hold my baby and even get out of bed due to the pain I feel. I hurt in all my joints, my back, my neck and I have leg pains that put me on my knees and unable to walk. My feet and ankles swell, my arms, fingers, and toes tingle with pain. I sometimes drop things because I can’t squeeze my fingers together to hold them. I am experiencing night sweats, hot flashes, nausea, and abnormal weight loss. I have dropped 90 pounds in 15 months. My stomach hurts every day and I never feel hungry. I have so many other symptoms, I feel as though I’m falling apart. I am working with my doctor now to try and find answers. I want to find quality in my life again. I want to feel good when I wake up and not have to lay in bed for at least an hour (waiting for pain meds to kick in) before I can move. Most importantly, I want to be able to pick my baby up out of her crib and hold her and not cry because it hurts my body so bad.

I am in the beginning stages of trying to figure out why I feel this way. I have had blood work drown which was good and I have a CT scan this week. It never even crossed my mind that all of this could be the side effects of taking Lupron as a child until I started reading other people’s stories. Please help?? What test do I need to take to help find answers? What meds are helping restore bone mass? What are other past Lupron patients experiencing and what is working to help them find quality in life again? Thanks in advance for your help!

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Image by AlexLoban from Pixabay.

This story was published originally on June 18, 2018.

Why Lupron is a Poor Diagnostic Tool for Endometriosis

by Philippa Bridge-Cook, PhD

Published on August 5, 2019

13362 views

In my work with The Endometriosis Network Canada, I have heard many women say that their doctors told them that if their pain does not go away on Lupron, then the pain must not be from endometriosis. Lupron never has and never will be an effective tool for diagnosing whether pain is due to endometriosis. Not only does Lupron have the potential for significant side effects, which alone should abrogate its use as a diagnostic tool, but it also is not at all effective at diagnosing endometriosis and distinguishing it from other conditions.

Lupron is a synthetic version of a naturally occurring hormone called gonadotropin-releasing hormone, and its action is actually stronger than the naturally occurring GnRH. It is a long-acting medication that initially stimulates hormones in the pituitary gland that control the menstrual cycle, and then suppresses these functions. It is typically given as a 1 month or 3 month injection.

Lupron Side Effects

Lupron therapy is associated with a significant potential for side effects. One of the biggest problems with Lupron is its effect on bone density (it can decrease bone density), and this effect is not always completely reversible after Lupron is discontinued. Lupron can also cause joint pain, which in some cases is permanent. Other potential side effects include hot flashes, vaginal dryness, headaches, mood swings, decreased interest in sex, depression (in some cases severe), cognitive problems, fatigue, acne, headaches, and upset stomach. Personal stories of women’s experiences of the downside of Lupron can be found here, here, here, here, and here.

Given all of these side effects, you might be wondering: why would anyone subject themselves to the potential for at best, a month of these side effects, and at worst, a lifetime of some of them, for the purpose of diagnosis? Even from the side effect perspective, using Lupron to try to diagnose endometriosis seems like a bad idea. But now we come to the more technical part of the discussion, which will address whether Lupron could even work as a diagnostic tool for endometriosis.

How to Evaluate a Diagnostic Tool

To evaluate the effectiveness of a diagnostic tool, the two measures that are used are called sensitivity and specificity. Sensitivity addresses the question of how often the diagnostic tool will pick up the disease, in people who have that disease. Specificity addresses the question of how often the test will be positive in people who actually do not have the disease (but may have conditions other than the one you are testing for). A good diagnostic test will pick up the presence of the condition in most people who have it, while not testing positive in people who may have similar symptoms but have a different disease. In other words, a good diagnostic test will have fairly high sensitivity and specificity.

All devices or tests that are approved by regulatory agencies as diagnostics have to undergo testing to demonstrate sufficient sensitivity and specificity. Lupron has not undergone such testing, because it was not developed as a diagnostic, and is not meant to be used as one. However, given the clinical trials that were done looking at the effectiveness of Lupron as a drug therapy, it is clear that the sensitivity and specificity of it as a diagnostic would not support its use in that way.

Lupron as a Diagnostic?

The clinical trial data published by the manufacturer in its prescribing information can be illuminating when considering its sensitivity and specificity for diagnosing endometriosis. The clinical trials used several measures to assess response to the drug, such as pelvic pain, dyspareunia (pain with intercourse), dysmenorrhea (pain with periods), and pelvic tenderness. The results showed that Lupron was by far the most effective at treating dysmenorrhea, compared to the other symptoms. Almost 90 percent of study participants had dysmenorrhea before taking Lupron, and after 6 months of treatment, fewer than 10 percent still had dysmenorrhea. (Not surprisingly, within 6 months after completing treatment, about 80 percent had dysmenorrhea again.) Looking at endometriosis symptoms other than pelvic pain, about 75 percent of study participants had pelvic pain at the start of the study, and 45 percent still had pelvic pain at the end. Lupron was similarly less effective at treating other symptoms of endometriosis.

From these results, we can get an idea of what the sensitivity of Lupron as a diagnostic would be. Imagine giving Lupron to a group of women with endometriosis, whose symptoms will vary from primarily dysmenorrhea, to all different types of pelvic pain at different times (or in some cases, all times) of the menstrual cycle. Those who have primarily dysmenorrhea will feel that their pain has been treated, whereas, because it is less effective on all other types of pain and symptoms, some women may feel that their pain did not decrease at all (remember, 45 percent of women still had pelvic pain after 6 months of Lupron). This is why it is completely incorrect for any doctor to say that if a woman’s pain did not decrease on Lupron, the pain cannot be from endometriosis. Therefore, the sensitivity of Lupron as a diagnostic for endometriosis is predicted to be poor, because in a significant number of women who actually do have endometriosis, it will not treat their pain substantially.

The specificity of Lupron as a diagnostic would be even worse. Clearly Lupron is effective at treating dysmenorrhea, because by its very mechanism of action it puts a woman into chemically-induced menopause, and you cannot have dysmenorrhea when you are not having periods. However, there are many causes of dysmenorrhea other than endometriosis. So even if Lupron does work to treat a woman’s pain (by preventing periods), this does not ensure that the cause of the pain was endometriosis.

A Call for More Research

There is no doubt that women would benefit greatly from a non-invasive diagnostic test for endometriosis, given that surgery is currently the only way to definitively diagnose it. However, Lupron is not sensitive or specific enough to be useful diagnostically. New diagnostic tests have been developed for many other diseases using recent advances in technology such as imaging methods, blood biomarkers, next generation sequencing, and others. A sensitive and specific diagnostic test for endometriosis is desperately needed. However, with so little funding going to basic and applied research into endometriosis, it is unlikely that this need will be met until this funding situation improves. As Siddhartha Mukherjee said about cancer in his book The Emperor of All Maladies:

“A disease needed to be transformed politically before it could be transformed scientifically.”

This is the situation that cancer research was in, during the 1940s, and sadly this is where we are at now, with endometriosis, a disease that affects one in ten women and has for centuries, in 2016.

We Need Your Help

More people than ever are reading Hormones Matter, a testament to the need for independent voices in health and medicine. We are not funded and accept limited advertising. Unlike many health sites, we don’t force you to purchase a subscription. We believe health information should be open to all. If you read Hormones Matter, like it, please help support it. Contribute now.

Yes, I would like to support Hormones Matter.

Image by Triggermouse from Pixabay.

This article was published originally on March 14, 2016.

Lupron Induced Osteoporosis?

by Samantha Bowick

Published on December 13, 2017

9778 views

Women who suffer with endometriosis do not have many options for treatment. As a result, many women try Lupron because they are desperate to be pain and symptom free. I was one of these women. In 2011 and 2013, I tried Lupron for a total of three doses and wish I knew then what I know now.

In 2010, I was diagnosed with endometriosis laparoscopically. After that, I tried everything from many different types of birth controls and pain medications to depression medications that can also be used to treat pain. Nothing worked. My doctor at the time suggested Lupron to me and I was desperate. I felt like I had already put my life on hold long enough because of this disease and just wanted to be out of pain. However, now I feel like I am suffering the consequences and it didn’t even get rid of my pain.

In 2015, I was diagnosed with osteoporosis. Prior to this, I had never had a bone scan done, not even before being administered Lupron. In 2009, I was diagnosed with Vitamin D deficiency and have been taking a supplement ever since. Three months before being diagnosed with osteoporosis, I stress fractured my knee and was told at my age, it should not have happened. In 2014, I had a hysterectomy because of endometriosis; I couldn’t take the pain anymore and had disease on both ovaries.

Before this, I had never had bone problems or been told that I could. I blame Lupron and strongly believe using it as a treatment for endometriosis led to me having osteoporosis. At 27 years old, I am still trying to work with doctors to determine if there are any treatments I can do because people my age having osteoporosis is rare. Many medications women use for osteoporosis could negatively impact my bones even more because of my age. If I don’t use any treatment, I could suffer from even more fractures or bone breaks the older I get. Right now, my average T-score for my left hip is -3.6 and was -3.3 when I was first diagnosed. I have no idea when my bones became so brittle. In my case, I wish I would have never tried Lupron as now I know this is one of the many side effects of this terrible treatment for endometriosis and something I will have to deal with for the rest of my life.

There are not studies done on medications for osteoporosis in my age group because there are not enough people with the disease to study. The medications my current doctor wants me to try would be a daily injection I would give myself in the abdomen for two years. They are known to possibly cause osteosarcoma, a bone cancer. Based on my history, I don’t like my odds. At this time, I don’t know how I will try to treat osteoporosis. I am planning on looking into natural ways of treating the disease and see how that goes.

As a result from my knee injury two years ago, I had to have an arthroscopic surgery. My doctor repaired my torn meniscus and removed scar tissue. It is taking me longer to heal than I anticipated and I wonder if it is because I have osteoporosis.

If doctors use Lupron for patients, they should be required to give these patients bone scans before their first dose and do follow ups yearly. It is a known fact that Lupron should not be administered in more than 12 doses over a patient’s LIFETIME. I wonder why this is?

I hope my story helps someone make a decision that is best for their body and raise awareness about Lupron. I am not a doctor, nor do I claim to be, but I am a patient that continues to live with the outcomes of having endometriosis.

We Need Your Help

Hormones Matter needs funding now. Our research funding was cut recently and because of our commitment to independent health research and journalism unbiased by commercial interests we allow minimal advertising on the site. That means all funding must come from you, our readers. Don’t let Hormones Matter die.

Yes, I’d like to support Hormones Matter.

Lupron Side Effects Survey Results Part One: Scope and Severity

by Chandler Marrs, PhD

Published on October 4, 2017

29679 views

Survey History

A few years ago, I embarked on a massive research project involving medication adverse reactions. I launched several online studies on the drugs that were popping up on our radar screen as having the most frequent and serious side effects; side effects that were largely ignored in the medical literature. At the time, this work was unfunded and, to a large degree, remains so today (feel free to contribute to our efforts). Despite the lack of funding, I thought it was important to investigate drug side effects from the patient’s perspective. Why was it that patients were reporting such a long list of devastating side effects while evidence in medical literature was largely absent? Were these patient experiences simply anomalies that we happened to be seeing, or was there something real going on? Without more quantitative data, these questions could not be answered.

To explore these questions, I designed several large studies, launched them online, and began collecting data, hoping that somehow the money would come in to fund the data analysis. It didn’t. And so these studies remained online, month after month, year after year, collecting data; data that needed to be analyzed and made public.

Earlier this year, I was fortunate to garner a grant for a new online project involving birth control and blood clots. The woman responsible for the grant understood the need to get the data from these legacy studies out to the public. The grant afforded me, not only the assistance of another researcher and a writer, but a much needed statistician. Per her wishes, the statistician could begin tackling the data analysis for these legacy studies, when not needed for the birth control project, e.g. during the periods of data collection. We are so very grateful that she recognized the importance of these projects.

A Note about the Data Sets

The surveys I designed were comprehensive, the data sets are massive and because they were conducted using survey software not designed for such large projects, the data sets are messy and require a tremendous amount of preparation to do even the most basic statistics. Notwithstanding the help of a part-time statistician, it will take us some months to ferret through these data sets. Nevertheless, we will get the data out. Again, if you’d like to help expedite this process, funding for a full-time statistician or even multiple statisticians would be most welcomed.

Beginning with Lupron

First in line, is one of my least favorite drugs used in women’s healthcare: Lupron. For those new to our blog, we’ve written a lot about Lupron over the years. Lupron or Leuprolide is a GnRH agonist prescribed for endometriosis, uterine fibroids, cysts, undiagnosed pelvic pain, precocious puberty, during infertility treatments, and to treat some cancers. I am not a big fan of this drug. If you have read the personal stories of the devastation caused by Lupron, or the research showing the mechanisms by which it induces damage, I doubt you would be either. Despite the decades of anecdotal evidence of serious side effects and the bevy of lawsuits filed and/or settled there is very little quantitative research delineating the scope and severity of these side effects. Given that Lupron chemically castrates its recipients, diminishing gonadal hormone production entirely, we might expect a little more research and certainly more caution in prescribing this drug. This doesn’t appear to be the case, as tens of thousands of women, men, and even children are prescribed this drug every year and have been for decades. Perhaps this is because Lupron is profitable, very profitable. In 2015, Lupron netted its manufacturers over $800 million in revenue.

What I find striking about Lupron, is not that are very few studies to support its safety and efficacy, or even that its manufacturers have been embroiled in lawsuits for decades all the while maintaining its safety and efficacy: that is common practice in the pharmaceutical industry. What is striking about Lupron is that it is a drug that effectively shuts down gonadal steroidogenesis, a key component of human health, and only a few in the medical industry think this is problematic. Here is a drug that could be used to induce chemical castration in pedophiles and rapists, if that were considered ethical or safe (and it’s not), but is used in tens of thousands of women, year in and year out, under the auspices of an effective treatment, and sometimes, even as a diagnostic for endometriosis. Worse yet, it is used on children in cases of precocious puberty, and to spur growth; two completely contraindicated uses.

How is that a drug that blocks hormones so completely, hormones that have receptors and therefore regulatory roles in every tissue and organ of the body (brain, nervous system, heart, GI system, fat cells, immune cells, muscle, pancreas, gallbladder, liver ) be considered safe? distribution of estrogen receptors Am I missing some great medical insight that suggests we really don’t need those pesky hormones after all; that all of those hormone receptors located all over the brain and body are there just because? How can a drug like this be used so cavalierly in young women? I don’t have answers for those questions beyond a collective insanity that has permeated medical science where women’s health is concerned. Absent answers, however, what I can begin to provide are data regarding the scope and severity of potential side effects associated with this drug; data gathered from the women themselves, unfiltered by industry bias or potential economic gains. Indeed, I suspect, once the full results of this study are published, industry will be none too happy with me or with our little project. Cue trolls.

All snark aside, results from this project, and from our others studies, are critical to an emerging discussion about medication safety. Patient experiences tell us a great deal about drug safety and efficacy, if we ask. I think it’s high time that we begin asking.

Study Design

The Lupron Side Effects Survey was designed to assess potential side effects across all organ systems. Hormones have receptors everywhere: it stands to reason then, if we deplete those hormones rapidly and continuously, there will be effects wherever those hormones play regulatory or modulatory roles. Of course, since estradiol, the primary hormone affected by Lupron, is critical to mitochondrial morphology, and thus mitochondrial energetics, anywhere there are high demands for energy, the nervous system, the heart, GI, musculature, we might anticipate a high degree of effects in those systems as well, especially with longer term use and as the damage accrues.

What we didn’t know, and won’t until we fully analyze the data (what is presented here is only the beginning), is in which systems the side effects are most severe (do they follow the path of mitochondrial energetics or some other yet to be identified pattern ) and when (do they present early or late, relative to use?); which women were more likely to have side-effects (are there health characteristics that make side effects more likely or more serious?); is there a dose-response curve for side effects (do higher doses mean greater side effects – sometimes with hormones, this isn’t the case); or how the side effects cluster together (did they cluster by organ or tissue system or by some other variable, like energy demands?). Most importantly, we didn’t know whether Lupron was clinically effective at reducing the symptoms for which it was prescribed. There is some evidence to suggest that while pain symptoms associated with endometriosis may show a statistically significant reduction, particularly while the woman is taking the drug, the reduction was neither clinically meaningful nor long lasting. That is, symptoms may diminish by a few points on a pain scale while on the drug, but not abate completely, and then inevitably return upon cessation. In light of the potential side effects induced by this medication, one would expect nothing less than a large clinical reduction, even remediation of the disease process itself, as the only fair trade off. It is not clear whether Lupron can provide those benefits. None of these questions have been answered in the medical literature, despite the use of this drug for many decades.

Lupron Side Effect Survey Basics

The study was launched in 2013. The goal was to get 500 respondents, evaluate, redesign and relaunch follow-up studies. We reached the 500 respondents within a few months, but absent funding, were not able to perform the analyses. So I left the study up to collect data passively (no longer advertising it), until recently.

When we closed the study, we had over 1400 partially completed surveys. For robustness, we analyzed only those surveys that were over 90% complete. That netted data from over 1000 respondents (the number of respondents for each question varies and is listed below with each item). The survey was anonymous, voluntary, and included informed consent.

Survey respondents were asked to provide basic demographic information, answer questions about pre-existing conditions, reasons for Lupron prescription, Lupron dosage, and degree of efficacy pre, during, and post Lupron usage. To capture the range and severity of potential side effects, survey respondents were asked to indicate the presence/absence and severity of symptoms experienced relative to their Lupron usage with a 0-4 Likert-type scale (0=None, 1=Mild, 2=Moderate, 3=Severe and 4=Life threatening). And yes, we recognize that ‘life-threatening’ is not an appropriate indicator for some types of symptoms. For consistency, however, we used the same rating scale across symptoms. One hundred and eighty possible symptoms were assessed.

This post will review range and severity of Lupron side effects. Subsequent posts will address efficacy, side-effect clustering, patient characteristics predicting side effects, side-effect dose-response curves and other topics.

Demographics

Survey respondents (n=1064) were largely Caucasian – 86.6% (African American -4.7%, Hispanic -2.6%, Other – 2.3%, Asian – 2%, American Indian/Alaska Native 1.6%) and educated (30% – some college, 34% – BA/BS, 15% – MA/MS). The average age of the survey respondent was 35.36 (SD – 8.63), while the average age at which Lupron was prescribed was 29.9 (SD – 8.2). Among these respondents, Lupron was most commonly prescribed for endometriosis (88%), painful periods (33.5%), heavy bleeding (26%), ovarian cysts (18%), PCOS (4%), IVF (4%), anemia (3.9%), breast cancer (1%), ovarian cancer (.4%), precocious puberty (.2%), other (8%). Respondents could select multiple answers.

For the discussion that follows, see the interactive graphic below. We will be discussing symptom categories from left to right. The categories of side effects are grouped, to some extent, by system involved or by symptom characteristics. To view the side effects, click any of the boxes below. The side effects within that category will appear, along with the number of respondents who answered that question. Click again on a particular side effect and the severity of the side effect is displayed by percentage of women who experienced each severity level. Click in the white space within the graphs to move up a level (note, this is a little tricky in the categories with lots of symptoms). The size of the graphic does not display well on mobile phones and/or when using the internet browser Internet Explorer. For the best viewing, please use a computer screen.

Patient Reported Side Effects Associated With Lupron

General Side Effects and Allergic Reactions

Compared to the frequency and severity of other symptoms experienced in association with Lupron, side effects relative to the injection itself and those that would be characterized as allergic reactions, itching, swelling, etc., were uncommon in most of the respondents, except for injection site pain, which was experienced in varying degrees of severity by over 70% of the respondents.

Sex and Libido

As one might expect with medication that chemically castrates its users, reductions in libido and other symptoms whose net result diminishes sexual interest and ability were common. Some degree of a loss of interest in sex was experienced by all but 23% of the women, with 38% reporting a severe diminishment in sexual interest. Nearly 44% of respondents reported moderate to severe pain during sex which may explained to some degree by the almost equal percentage of women reporting moderate to severe vaginal dryness. Other symptoms reported included breast pain, swelling, and to a much lesser extent, discharge.

Muscle and Joint Pain

Up to 50% of the women reported moderate to severe muscle and/or joint pain. This is notable inasmuch as for the majority of the women prescribed Lupron, pelvic and abdominal pain associated with endometriosis is the driving factor for the use of this drug. It appears that we may be trading pain in one region of the body for another.

Gastrointestinal and Related Symptoms

Here again we see that a large percentage of women (from 15-50% depending upon the symptom) report moderate to severe gastrointestinal disturbances from nausea, vomiting and diarrhea through constipation and even bowel obstruction. Moderate to severe bladder pain was common (~31%) as was difficulty in urination (~19%) and bladder control (~18%). Since bladder pain and interstitial cystitis are co-morbid with endometriosis, it is difficult to determine if these symptoms were precipitated or exacerbated by the Lupron or simply associated with the endometriosis and thus, not remediated by the medication. We will attempt to disentangle those relationships with further data analysis and in subsequent studies.

Of note, gallbladder disease (~6.2% – all categories combined), gallstones (~3%), kidney disease (2%), kidney stones (4.5%) and renal failure affect a smaller but noticeable number of Lupron recipients. This consistent with adverse event reporting elsewhere. Similarly, non-alcoholic fatty liver was noted in ~6.6% of the survey respondents.

Bone, Skin, and Related Symptoms

Bone formation is particularly hard hit by the diminishment of estradiol. Bone related symptoms are some of the most commonly reported side effects ascribed to Lupron. Research suggests Lupron induces a 5-6% decline in bone mineral density over just 6-12 months of use. Read more on the mechanisms by which Lupron induces bone loss.

Almost 20% of the women who completed the survey reported some degree of osteoporosis, and 16% reported cracking or brittle bones, 42% reported toothaches (9% severe) and 26% had cracking teeth. Osteonecrosis was reported by 3% of the respondents. Skin and hair symptoms were common and affected a sizable percentage of the respondents as well. What we failed to ask about were fractures in the spine and pelvis or osteoporosis in the jaw; side effects that commonly appear in post Lupron discussion boards. We will do so in subsequent surveys.

Temperature Dysregulation

As expected by a drug that induces a rapid menopausal state, vasomotor symptoms with temperature dysregulation were prominent afflicting ~90% of the respondents. Severe hot flashes and night sweats were reported by over half of the study population.

Metabolic Symptoms

Estradiol affects insulin regulation and general metabolism, so it stands to reason that if concentrations are diminished significantly, metabolic disruption would ensue. Hypoglycemia was reported by about 15% of the women, while hyperglycemia was reported by about 6%. Similarly, increased hunger and thirst were prominent at least 50% of the population, along with rapid weight gain (mild 19.2%, severe 25.9%). In contrast, rapid weight loss was reported by 12% of the respondents. New onset diabetes, Type 1 and Type 2 was reported by ~1% and 2.8% respectively. As we perform more advanced analyses, we will try to more fully characterize the metabolic changes in different groups of women.

Cardiovascular and Respiratory Symptoms

We know that the estrogens and androgens affect heart function via multiple mechanisms, both at the receptor level and via more global changes to mitochondrial functioning. What we don’t know is what impact blocking those hormones so abruptly and completely and sometimes even chronically, has on heart function. Clinically, the results of this survey point to dysregulated blood pressure (BP – 12.5%) and heart rate or rhythm (24.7%) with a trend towards the elevated measures for blood pressure (24.4% – all, 13.3% moderate to life threatening) and heart rate (27.7% – all, 22% moderate to life-threatening. However, there was a noticeable percentage of women who experienced lower blood pressure (16.4%) and heart rate (6.1%). At least 10 women experienced a heart attack, 36 women developed mitral valve prolapse, 10 women developed blood clots in the leg and 8 women had pulmonary emboli. Difficulty breathing and sleep apnea were reported by 22.2% and 15.6% respectively. As we do further analyses we’ll be able to more fully characterize the pattern of cardiovascular symptoms.

Brain and Nervous System Symptoms

The next five sections of the graphic represent the scope and severity of symptoms associated with the nervous system. Though categorized distinctly for purposes of display, the distinctions are somewhat arbitrary as the symptoms within each category represent those related to the brain and nervous system. Arguably, many of the cardiovascular symptoms discussed previously may also represent nervous system symptoms, possibly suggesting some degree of autonomic system dysregulation.

Headache, Migraine, Dizziness, and Seizures. A large percentage of women experienced headache and migraine pain, frequently rated as severe or life-threatening (27.2% and 28.3% respectively). Dizziness was common (69.4%), as was vertigo (46.9%). Sleepiness (68%) and fatigue (87.3) were common, but interestingly, also insomnia (76.4). Seizures reported by 5.1% of respondents. Falling (17.1%) and difficulty walking (27.9%), perhaps indicating balance issues, were also reported. TIAs were reported by 11 women and full strokes by 3 women. (Nervous System Symptoms).

Myoclonus and Neuropathy. Shaking, jerking, numbness, spasms and tingling were experienced to some degree by 15%-35% of the survey respondents. A sizable percentage of women reported moderate to severe symptoms. Muscle weakness was reported by 11-34% of the respondents whereas limb and/or facial paralysis was experienced 3-4% of the women. (Neuromuscular, Sensory Perception and Motor Control).

Hearing and Vision Disturbances. Some degree of blurred vision was experienced by 46.5% of the women, with a little over 20% rating the symptom moderate to severe. Partial loss of vision was reported by almost 10% of the women, half of them indicating moderate to severe loss. Similarly, almost 20% reported some hearing impairment. Similarly, hypersensitivity to light or to sound was indicated by 35% and 37.5% respectively. (Sensory and Motor Symptoms).

Speech and Language Disturbances. Fully 20-50% of the respondents reported difficulty with basic communication, everything from difficulty speaking and finding words to difficulty understanding speech, reading and writing. (Sensory and Motor Symptoms).

Mood, Memory, Mental Health and Affective Behavior. The brain is a major target of and source for steroid hormones. Estrogen receptors are co-localized on neurons and affect neurotransmission, neurite outgrowth, synaptogenesis and myelin growth and estradiol is generally considered neuroprotective. The prefrontal cortex, hippocampus, and amygdala, responsible for regulating directed behavior, memory, and emotion, have high densities of estrogen receptors. Depleting estradiol would be expected to have a significant impact on these functions, and it did. It is here that we see some of the most troubling and least well appreciated (by the medical profession) side effects associated with Lupron. A significant percentage of women reported severe psychological disturbances ranging from depression and anxiety (>50%) to suicidality (15% severe to life-threatening). Visual or auditory hallucinations were experienced by ~12%, with >6% reporting moderate severe issues. Moderate to severe frontal cortex issues like dulled or inappropriate emotions, lack of motivation, impulsiveness were reported in 25% to over 50% of respondents. Moderately to severely altered mental states (delirium, disorientation, confusion) were reported by 6%-25% of the women. Moderate to severe diminishment in memory capacity was reported by at least a third of the women. This is in addition the difficulties with language reported above. (Mood, Memory and Mental Health).

General Impressions

Consistent with the case stories and patient comments on message boards related to Lupron side effects, the majority of women feel rotten while on this drug. This is to be expected given the global distribution of estrogen receptors. The brain and nervous system seem particularly hard hit. Again, this is understandable given the density of estrogen receptors in the brain and the modulatory role it, and other steroid hormones, play in neurotransmission. By depriving the estrogen receptors of their cognate ligand, estradiol, Lupron fundamentally alters brain chemistry, abruptly and thoroughly. Perhaps even more troubling, estradiol is required for mitochondrial functioning. By depleting estradiol, the mitochondria are impaired, and with that impairment comes a long line of compensatory mechanisms that will ultimately derail not only mitochondrial capacity but also the capacity of all of the cell functions that require healthy mitochondria. The fact that we see such severe side effects attributable to nervous system function would be expected with estradiol depletion.

We Need Your Help

This post was published originally on Hormones Matter on September 1, 2016. Since then, we have lost our funding to complete this and the other ongoing studies. We have enormous data sets like this one on medication adverse reactions waiting to be analyzed and published. Without funding, however, these data will never see the light of day. If these issues are important to you, please contribute. If you know of an organization or benefactor interested in understanding short and long-term medication and vaccine reactions, please refer them to us.

Yes, I’d like to support Hormones Matter.

Photo by Diana Polekhina on Unsplash.

Adverse Reactions, Hashimoto’s Thyroiditis, Gait, Balance and Tremors

by Chandler Marrs, PhD

Published on July 6, 2017

69807 views

Gait, tremors with adverse medication vaccine reactions

One of the things I most love about social media and health research is the opportunity to identify patterns of illness across different patient groups. Here is an example of finding research from one patient group, ThyroidChange, that likely spans many others (Gardasil injured, post Lupron Hashimoto’s, and Fluoroquinolone reactions – to name but a few) and offers clues to a perplexing array of symptoms. The research, is about a little known association between movement and balance disorders and Hashimoto’s thyroiditis: Ataxia associated with Hashimoto’s disease: progressive non-familial adult onset cerebellar degeneration with autoimmune thyroiditis. Some background.

Hashimoto’s Disease

Hashimoto’s is the most common causes of hypothyroidism afflicting women at a rate of 10 to 1 compared to men. It is an autoimmune disorder in which antibodies attack the thyroid gland and destroy its ability to maintain normal thyroid hormone concentrations. The most common symptoms include: fatigue, muscle pain, weight gain, depression, cognitive difficulties, cold intolerance, leg swelling, constipation, dry skin. If left untreated, goiter – a swollen thyroid gland, appears. If left untreated for an extended period, cardiomyopathy (swelling of the heart muscle), pleural (lung) and pericardial (heart) effusion (fluid), coma and other dangerous conditions develop.

Hashimoto’s and Cerebellar Degeneration

A little known risk in Hashimoto’s is cerebellar degeneration. The cerebellum is the cauliflower looking section at the base of the brain that controls motor coordination – the ability to perform coordinated tasks such as walking, focusing on a visual stimuli and reaching for objects in space. The walking and balance disturbances associated with cerebellar damage or degeneration have a very distinct look, a wide gait, with an inability to walk heel to toe. Cerebellar ataxia looks like this:

In recent years, cerebellar involvement in attention and mood regulation have also been noted. The physicians reporting the Hashimoto’s – ataxia connection present case studies of six patients with Hashimoto’s disease, presumably controlled with medication and a progressive and striking shrinkage of the cerebellum (see report for MRI images) along with progressively debilitating ataxia (walking and balance difficulties) and tremors. Here’s where it becomes interesting.

Hashimoto’s: Medication Adverse Reaction and Misdiagnosis

Hashimoto’s disease is prevalent in our research into medication adverse reactions for Gardasil and Cervarix and Lupron, with some indications it may develop post Fluoroquinolone injury as well. The symptoms are difficult to distinguish from other neurological and neuromuscular diseases such as chronic fatigue syndrome, fibromyalgia, multiple sclerosis and an array of psychiatric conditions, and so Hashimoto’s often goes undiagnosed or is misdiagnosed and mistreated for some time.

Hashimoto’s, Demyelination and Cerebellar Damage

In some of the more severe adverse reactions to medications and vaccines that would lead to Hashimoto’s, the tell tale cerebellar gait disturbances have been noted and documented, along with a specific type of tremor (discussed below).

Research from other groups shows a strong relationship between thyroid function and myelin/demylenation patterns in nerve fibers in animals. Specifically, insufficient T3 concentrations demyelinates nerve axons, while T3 supplementation elicits myelin regrowth. Myelin is the white sheathing, the insulation that protects nerves and improves the electrical conduction of messages in sensory, motor and other neurons. Like co-axial cable in electrical wiring, when the protective sheathing is lost, electrical conductance is disrupted. The early symptoms of a demyelinating disease neuromuscular pain, weakness, sometimes tremors. These can be misdiagnosed as multiple sclerosis, fibromyalgia, chronic pain, when in reality, the culprit is a diseased thyroid gland.

Back to the Cerebellum

The cerebellum is a focal point of white matter axons – myelinated sensory and motor nerves. The cerebellum is where input becomes coordinated into motor movements or movement patterns. White matter damage in the cerebellum causes cerebellar ataxia, the movement and balance disorders displayed above. Hashimoto’s elicits white matter disintegration. Adverse reactions to medications and vaccines can elicit autoimmune Hashimoto’s disease. See the connection?

The Thiamine – Gut Connection

It gets even more interesting when we add another component of systemic medication adverse reactions – nutritional malabsorption, specifically thiamine deficiency. Almost across the board, patients with medication or vaccine adverse reactions report gut disturbances, from leaky gut, to gastroparesis, constipation, pain and a myriad of other GI issues that make eating and then absorbing nutrients difficult. Gut issues are common in thyroid disease too.

As we learn more, and as individuals are tested, severe nutrient deficiencies are noted, in vitamin D, Vitamin B1, B12, Vitamin A, sometimes magnesium, copper and zine. We’ve recently learned of the connections between Vitamin B1 or thiamine deficiency and a set of conditions affecting the autonomic nervous system called dsyautonomia or Postural Orthostatic Tachycardia Syndrome (POTS) linked to thiamine deficiency in the post Gardasil and Cervarix injury group. It may be linked to other injured groups as well, but we do not know yet.

Thiamine and Cell Survival

Thiamine or vitamin B1, is necessary for cellular energy. It is a required co-factor in several enzymatic processes, including glucose metabolism and interestingly enough, myelin production (the Hashimoto’s – cerebellar connection). We can get thiamine only from diet. When diet suffers as in the case of chronic alcoholism, where most of the research on this topic is focused, or when nutritional uptake is impaired, thiamine deficiency ensues. Thiamine deficiency can elicit cell death by three mechanisms:

Mitochondrial dysfunction (reduced energy access) and cell death by necrosis
Programmed cell death – apoptosis
Oxidative stress – the increase in free radicals or decrease in ability to clear them

Thiamine deficiency in and of itself can elicit a host of serious health symptoms. The cell death and disruption of cellular energy balance can be significant and lead to a totally disrupted autonomic system.

Thiamine and Myelin Growth

Add to those symptoms, the fact that thiamine is involved in the growth myelin sheathing around nerves, and we have a whole host of additional neuromuscular symptoms masking as fibromyalgia, multiple sclerosis, chronic fatigue. Like with MS, limb and body tremors are noted in dysautonomic syndromes such as POTS. (Video of POTS tremors, note the uniqueness of the POTS tremor and the similarity between it and the foot tremor shown above along with cerebellar ataxia).

Let thiamine deficiency continue unchecked for period and we get brain damage, as white matter – the myelin disintegrates in the brainstem, the cerebellum and likely continues elsewhere. One of the most prominent areas of damage in thiamine deficiency, is the cerebellum, and hence, the cerebellar ataxia (movement disorders) noted in chronic alcoholics who are thiamine deficient, but also observed post medication or vaccine adverse reaction.

The Double Whammy on Myelin and Cerebellar Function

In the case medication or vaccine adverse reactions, particularly those that reach the systemic level, we have a double whammy on myelin disintegration: from a diseased thyroid gland and a diseased gut. Hashimoto’s and the reduction of thyroid hormones, particularly T3, impairs nerve conduction by shifting from a constant and healthy remyelinating pattern to one of demyelination, while the lack of thiamine further impairs myelin regrowth, because it is a needed co-factor. Both deficiencies affect peripheral nerves, but both also hit the brainstem, the cerebellum and likely other areas within the brain.

Take Home Points

The science of adverse reactions is new and evolving and much of what I am reporting here remains speculative. However, it has become abundantly clear through our research that to address medication adverse reactions or vaccine adverse reactions in a simplistic fashion, by region, or in an organ specific manner, is to miss the broader implications of the compensatory disease processes that ensue. Moreover, to look for symptoms of adverse reactions simply by the drug’s mechanism of action and/or by the standard outcome variables listed in adverse event reporting systems, again misses the complexity of the human physiological response to what the body is perceiving as a toxin. I believe that the entire framework for understanding the body’s negative response to a medication must be shifted to a much broader, multi-system, and indeed, multidisciplinary approach. In the mean time, we will continue to collect data on adverse reactions and offer our readers points of consideration in their quests for healing. I should note, that finding these connections is entirely contingent on the input our community of patients and health activists, both via the personal health stories that so many of you have been willing to share and the data we collect through our research. You know more about your health and illness than we do.

What we Know So Far – Tests to Consider

If you have had an adverse reaction to a medication or vaccine and neuromuscular difficulties, like pain, numbness, motor coordination problems, tremors etc., consider testing for Hashimoto’s thyroiditis. Also, consider thyroid testing when fatigue, depression, mood lability (switching moods), constipation, attentional and focus difficulties are present. In fact, I would consider thyroid testing, specifically for autoimmune thyroid disease like Hashimoto’s, as one of the first disease processes to rule out.

If you have had an adverse reaction to a medication that includes gut disturbances, consider the possibility that you are deficient in key micronutrients such as Vitamin D, the B’s, Vitamin A, magnesium, copper, zinc. And given the modern diet, consider that you were probably borderline deficient even before experiencing the adverse reaction. These nutrients are critically important to health and healing (and no, I do not have an association with vitamin companies or testing companies). Some tests for these nutrients are more accurate than others, so be sure to do your homework first.

If you have symptoms associated with autonomic systems dysregulation such as those associated with POTS, dysautonomia and its various permutations, consider thiamine testing, especially, transkelotase testing.

Share Your Story

If you have experienced a reaction to a medication or vaccine, please share your story in a blog post. Write for us.

We Need Your Help

If you think what we do is worthwhile, contribute to research and our medical reporting at Hormones Matter. We’re totally unfunded at this point and can use your help to continue operations. Yes, I’d like to support Hormones Matter.

Image Source: Pixabay.

Postscript: This article was published originally on Hormones Matter on October 15, 2013.

Lupron for Fibroids: Does It Work? Not for Me.

by Heather

Published on April 4, 2017

7570 views

The second week of November 2016 was disappointing to say the least, but I was hopeful as I walked into the massive, world renowned hospital to finally get the fibroid removed that had been wrecking my life. Bleeding nearly every day for over a year, I had become increasingly fatigued. I was forced to curb usual activities due to the frequent near hemorrhage loss of blood.

About a month prior, I met a surgeon who assured me that he could remove the apparent submucosal fibroid. This meant I would be getting my life back, at last. He did warn me that there was a 5% chance that I would require an additional surgery if he could not remove the entire tumor the first time. I was so hopeful and relieved. If this were successful, there were so many things that I would be able to do without worrying about severe cramping, bleeding and fatigue. I felt elated, and happily agreed to participate in a fibroid research study, because I wanted to do whatever small thing I could to help other women with similar conditions get the best type of medical care, perhaps avoiding a hysterectomy or receiving ineffective treatment.

I awoke from surgery with the discouraging news that they were unable to remove the entire growth. My surgeon ordered a “hormone shot” that would help with the bleeding and shrink the fibroid. I was told that I might have hot flashes. In my less than alert state, I agreed. I had previously been quite vocal about my disinterest in medical therapy. The Mirena IUD that another ObGyn placed nearly two years prior had done nothing to help. A nurse administered an injection of the three-month dose of Lupron Depot just before I left the hospital.

A few days later, I began experiencing insomnia, headaches, heart palpitations, emotional liability, and intense hunger, all as the heavy bleeding continued. A month went by and the bleeding stopped. Severe migraines, neck pain, and brain fog developed. I could barely function. It was the holiday season, but I felt less than merry. I could barely focus. I experienced episodes of amnesia, night sweats and began to have spine pain and ligament pain in my arms and legs.

Seeing a chiropractor helped my neck. Calcium and magnesium supplements, lots of water and improving my diet did make a small difference. Still it was pretty unbearable. I contacted the hospital asking if these symptoms were side effects of the Lupron and what might help. A nurse sent me a message saying that none of my symptoms were due to the Lupron. Great I thought, this is the modern day version of hysteria? They think I am making this up?

I later spoke to an intern and another surgeon who told me that what I was experiencing were in fact common side effects of Lupron. They both told me they were sorry. Norethindrone was prescribed. By this time, I was just two weeks away from my second surgery. The hot flashes subsided slightly, but the other symptoms persisted. The day before my surgery I had a hysteroscopy and found out that my fibroid had not shrunk at all. My surgeon said he had his work cut out for him. I wanted to choke him a little. He was my only hope so I begged him to do his best.

This second surgery was successful! A relief, but unlike other times, the lack of hormones from the Lupron seemed to prolong recovery. My legs were swollen for days and the post anesthesia effects lingered for weeks.

Three months came and went but the “side effects” have not gone away. The deep bone pain disrupts my sleep and limits physical activity. At times it is difficult to be cheerful or even relatively pleasant. I am notably forgetful. I’m only able to do a small fraction of what was possible before the Lupron, even with a large fibroid. Although things didn’t go as planned, I hope that sharing my experience will help someone else have a better one.

lupron side effects - Page 2

Post Lupron Symptoms

Multiple Sclerosis or Something Else?

Another Surrogacy and Another Round of Lupron

Share Your Story

We Need Your Help

Related posts:

You might be interested in

Steroid Hormones and Metabolic Flexibility: A Critical Factor in Post Lupron and Post Oophorectomy Ill Health

Mitochondria

Metabolic Flexibility: Adapt and Survive

Estradiol Equals Increased Mitochondrial Efficiency and Decreased ROS

Estradiol, Pyruvate, and ATP

What about Natural Declines in Estradiol?

Metabolic Flexibility and Tissue Type

Final Thoughts

We Need Your Help

Related posts:

You might be interested in

We Need Your Help

Related posts:

You might be interested in

Lupron Side Effects

How to Evaluate a Diagnostic Tool

Lupron as a Diagnostic?

A Call for More Research

We Need Your Help

Related posts:

You might be interested in

We Need Your Help

Related posts:

You might be interested in

Survey History

A Note about the Data Sets

Beginning with Lupron

Study Design

Lupron Side Effect Survey Basics

Demographics

Patient Reported Side Effects Associated With Lupron

General Side Effects and Allergic Reactions

Sex and Libido

Muscle and Joint Pain

Gastrointestinal and Related Symptoms

Bone, Skin, and Related Symptoms

Temperature Dysregulation

Metabolic Symptoms

Cardiovascular and Respiratory Symptoms

Brain and Nervous System Symptoms

General Impressions

We Need Your Help

Related posts:

You might be interested in

Hashimoto’s Disease

Hashimoto’s and Cerebellar Degeneration

Hashimoto’s: Medication Adverse Reaction and Misdiagnosis

Hashimoto’s, Demyelination and Cerebellar Damage

Back to the Cerebellum

The Thiamine – Gut Connection

Thiamine and Cell Survival

Thiamine and Myelin Growth

The Double Whammy on Myelin and Cerebellar Function

Take Home Points

What we Know So Far – Tests to Consider

Share Your Story

We Need Your Help

Related posts:

You might be interested in

Related posts:

You might be interested in